Unidirectional block and reentry of cardiac excitation: a model study.
A computer model of a ring-shaped, one-dimensional cardiac fiber was used for examination of responses of propagation to premature stimuli applied under different degrees of both cell-to-cell coupling and membrane excitability. Results demonstrated the importance of cellular uncoupling in the genesis of unidirectional block and reentry. Propagation of excitation itself created a certain degree of functional inhomogeneity that provided necessary conditions for unidirectional block and reentry. The likelihood of induction of unidirectional block was proportional to the degree of cellular uncoupling. In contrast, uniform reduction in sodium channel conductance decreased the inducibility of unidirectional block. Nonsustained and sustained reentry was induced by a properly timed single premature stimulus during the refractory period of a propagating action potential. Reduction of the size of the reentry pathway resulted in an increased degree of interaction between the wavefront and its tail, which, in turn, changed the kinetics of the slow ionic channels, bringing about shortening of action potential duration. Alternans in action potential duration were also demonstrated during circus movement and were caused by the alternating kinetic properties of the slow ionic currents. Inhomogeneity along the reentry pathway in refractory period, in membrane excitability, in fiber cross-sectional area, or in gap junction resistance also provided conditions necessary for unidirectional block. The simulations suggested that an important role was played by cellular uncoupling in the genesis and maintenance of unidirectional block and reentry.
Quan
W
W
Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio 44106.
Rudy
Y
Y
D000200:Action Potentials; D000818:Animals; D006321:Heart / Q000503:physiopathology*; D006327:Heart Block / Q000503:physiopathology*; D006329:Heart Conduction System / Q000503:physiopathology; D006801:Humans; D008955:Models, Cardiovascular; D012032:Refractory Period, Electrophysiological